AIR QUALITY CRITERIA FOR PHOTOCHEMICAL OXIDANTS SUMMARY AND CONCLUSIONS U.S. DEPARTMENT OF HEALTH, EDUCATION, AND WELFARE Public Health Service Environmental Health Service ------- 3 AIR QUALITY CRITERIA FOR PHOTOCHEMICAL OXIDANTS (The summary and conclusions herein are reproduced from the original volume as identified on this page.) US EPA Headquarters and Chemical Libraries ; EPA West Bldg Room 3340 £ Mailcode 3404T £p 1301 Constitution Ave NW <£: Washington DC 20004 o- 202-566-0556 /* ^ U.S. DEPARTMENT OF HEALTH, EDUCATION, AND WELFARE Public Health Service Environmental Health Service National Air Pollution Control Administration Washington, D.C. March 1970 Repository Material !annanent Collection ------- Chapter 10. SUMMARY AND CONCLUSIONS A. INTRODUCTION This document is a consolidation and assessment of the current state of knowledge on the origin and effects of the group of air pollutants known as photochemical oxidants on health, vegetation, and materials. The purpose of this chapter is to provide a concise picture of the information contained in this document, including conclusions which are believed reasonable to consider in evaluating concentrations of photochemical oxidants which are known to have an effect on either health or welfare. Although nitrogen dioxide is considered one of the photochemical oxidants, it is to be subject of a separate report. Consequently, nitrogen dioxide is discussed in this document only to the extent that it participates in the formation and reac- tions of other photochemical oxidants. The information and data contained in this docu- ment comprise the best available bases, and provide the rationale for development of specific levels of standards of photochemical oxidants in the ambient ah- for protection of public health and man's environment. B. NATURE OF PHOTOCHEMICAL OXIDANTS Photochemical oxidants result from a com- plex series of atmospheric reactions initiated by sunlight. When reactive organic substances and nitrogen oxides accumulate in the atmo- sphere and are exposed to the ultraviolet component of sunlight, the formation of new compounds, including ozone and peroxyacyl nitrates, takes place. Absorption of ultraviolet light energy by nitrogen dioxide results in its dissociation into nitric oxide and an oxygen atom. These oxygen atoms for the most part react with air oxygen to form ozone. A small portion of the oxygen atoms and ozone react also with certain hydrocarbons to form free radical intermediates and various products. In some complex manner, the free radical intermedi- ates and ozone react with the nitric oxide produced initially. One result of these reac- tions is the very rapid oxidation of the nitric oxide to nitrogen dioxide and an increased concentration of ozone. The photochemical system generally is ca- pable of duplication in the laboratory. For various reasons, however, laboratory results cannot be quantitatively extrapolated to the atmosphere. Theoretically generation of an atmospheric simulation model should be feasi- ble, enabling the prediction of ambient oxi- dant concentrations from a knowledge of emission and meteorological data. The devel- opment of such a model, however, is depen- dent on the acquisition of more reliable and applicable quantitative information derived from direct atmospheric observations, as well as on the refinement of results obtained from. irradiation chamber studies. C. ATMOSPHERIC PHOTOCHEMICAL OXIDANT CONCENTRATIONS The presence of photochemically formed oxidants has been indicated in all of the major U.S. cities for which aerometric data have been examined. On a concentration basis, ozone has been identified as the major com- ponent of the oxidant levels observed. Diffi- culties arise, however, in interpreting data obtained by the most commonly used oxidant measuring method; this method is nonspecific and subject to several interferences. Adjusted oxidant concentrations, obtained by correc- ting potassium iodide oxidant measurements 10-1 ------- for known interferences, have been found to be relatively close to concurrent measure- ments of ozone alone. Since photochemical oxidants are the pro- ducts of atmospheric chemical reactions, the relationship between precursor emissions and atmospheric oxidant concentrations is much less direct than is the case for primary pollutants. A further complicating situation is the dependence of these photochemical reac- tions on intensity and duration of sunlight, and on temperature. In an analysis of oxidant concentration data for 4 years and 12 stations, the daily maximum 1-hour average concentration was equal to or exceeded 290 jug/m3 (0.15 ppm) up to 41 percent of the time; maximum 1-hour average concentrations ranged from 250 to 1,140 jug/™3 (0.13 to 0.58 ppm); short-term peaks were as high as 1,310 jug/™3 (0.67 ppm). Yearly averages, commonly app- lied to other pollutants, are not representative of air quality with respect to oxidant pollu- tion, because 1-hour average ozone concentra- tions will necessarily be at or about zero for approximately 75 percent of the time when photochemical reactions are minimal. Peroxyacyl nitrates, through not routinely measured, have been identified in the atmo- sphere of several cities. These compounds may be assumed to be present whenever oxidant levels are elevated. D. NATURAL SOURCES OF OZONE Ozone can be formed naturally in the atmosphere by electrical discharge, and in the stratosphere by solar radiation, by processes which are not capable of producing signifi- cant urban concentrations of this pollutant. Maximum instantaneous ozone levels of from 20 to 100 /ig/m3 (0.01 to 0.05 ppm) have been recorded in nonurban areas. E. MEASUREMENT OF PHOTOCHEMICAL OXIDANTS The most widely used technique for the analysis of atmospheric total oxidants is based on the reaction of these compounds with potassium iodide to release iodine. The iodine may then be measured by either colorimetnc or coulometric methods. Calibrating the oxi- dant measurement method used against a known quantity of ozone provides a measure- ment of the net oxidizing properties of the atmosphere in terms of an equivalent concen- tration of ozone. Most oxidant measurements are currently being made by the colorimetric method, although coulometric analyzers are used in a number of laboratory and field studies. In order to generate comparable data, it is essential that all measurements be made by techniques which have been calibrated against the same standard or reference method. Since at the present time there is no standard method for the determination of total oxi- dants, the National Air Pollution Control Administration recommends use of the neu- tral-buffered 1 percent potassium iodide col- orimetric technique as the method against which all instruments and other methods should be compared. In addition to serving as a manual procedure for determining oxidants, the reference method may be used in conjunc- tion with a "dynamic calibration" technique for instrumental methods. Reducing agents such as sulfur dioxide produce a negative interference in oxidant determination. Such interference can be re- duced, however, by passing the air stream through a chromium trioxide scrubber prior to measurement. Unfortunately, a portion of the nitric oxide which may be present in the air stream is oxidized to nitrogen dioxide by the scrubber. This results in an apparent increase in the oxidant measurement of about 11 percent of the concentration of nitric oxide. Moreover, a portion of the atmospher- ic nitrogen dioxide concentration will also contribute to the oxidant measurement. Per- oxyacyl nitrate concentrations are usually small and contribute only a very slight amount to the oxidant reading. There are several means for the specific measurement of atmospheric ozone. Instru- mental methods include chemiluminescent analysis based on the reaction of ozone with Rhodamine B, gas phase olefin titration, and 10-2 ------- ultraviolet and infrared spectroscopy. A semi- quantitative method for ozone measurement is based on its ability to produce cracks in stretched rubber. Peroxyacyl nitrates can be measured in the atmosphere by gas chromato- graphy with the use of an electron-capture detector. For a better evaluation of the results of research on the effects of photochemical oxidants, it is essential that data be obtained for individual oxidants such as nitrogen diox- ide, ozone, PAN, formaldehyde, acrolein, and organic peroxides. These data would either replace or complement data on total oxidants. Instrumentation currently available permits the accurate measurement of atmospheric ozone, nitrogen dioxide, and PAN. There exists, however, a further need to develop instruments capable of measuring other indi- vidual gaseous pollutants which have the properties of oxidants. Photochemical reac- tions and problems derived from oxidants can be much better defined using specific meth- ods for measurement in preference to the traditional total oxidants determination. F. EFFECTS OF PHOTOCHEMICAL OXIDANTS ON VEGETATION AND MICROORGANISMS Injury to vegetation is one of the earliest manifestations of photochemical air pollu- tion, and sensitive plants are useful biological indicators of this type of pollution. The visible symptoms of photochemical oxidant produced injury to plants may be classified as: (1) acute injury, identified by cell collapse with subsequent development of necrotic patterns; (2) chronic injury, identified by necrotic patterns with or without chlorotic or other pigmented patterns; and, (3) phsyiologi- cal effects, identified by growth alterations, reduced yields, and changes in the quality of plant products. The acute symptoms are generally characteristic of a specific pollutant; though highly characteristic, chronic injury patterns are not. Ozone injury to leaves is identified as a stippling or flecking. Such injury has occurred experimentally in the most sensitive species after exposure to 60 jug/m3 (0.03 ppm) ozone for 8 hours. Injury will occur in shorter time periods when low levels of sulfur dioxide are present. PAN-pro- duced injury is characterized by an under-sur- face glazing or bronzing of the leaf. Such injury has occurred experimentally in the most sensitive species after exposure to 50 jug/m3 (0.01 ppm) PAN for 5 hours. Leaf injury has occurred in certain sensitive species after a 4-hour exposure to 100 jig/m3 (0.05 ppm) total oxidant. Ozone appears to be the most important phytotoxicant in the photo- chemical complex. There are a number of factors affecting the response of vegetation to photochemical air pollutants. Variability in response is known to exist between species of a given genus and between varieties within a given species; varie- tal variations have been most extensively studied with tobacco. The influence of light intensity on the sensitivity of plants to damage during growth appears to depend on the phy- totoxicant. Plants are more sensitive to PAN when grown under high light intensities, but are more sensitive to ozone when grown under low light intensities. Reported findings are in general agreement that sensitivity of green- house-grown plants to oxidants increases with temperature, from 10° to 38° C (40° to 100° F), but this positive correlation may result from the overriding influence of light intensi- ty on sensitivity. The effects of humidity on the sensitivity of plants has not been well documented. General trends indicate that plants grown and/or exposed under high humidities are more sensitive than those grown at low humidities. There has been little research in this direction, but there are indications that soil factors such as drought and total fertility influence the sensitivity of plants to phytotoxic air pollutants. The age of the leaf under exposure is important in de- termining its sensitivity to air pollutants. There is some evidence that oxidant or ozone injury may be reduced by pretreatment with the toxicant. 10-3 ------- Identification of injury to a plant as being caused by air pollution is a difficult undertak- ing. Even when the markings on the leaves of a plant may be identified with an air pollut- ant, there is the further difficulty of evaluat- ing the injury in terms of its effect on the intact plant. Additional problems arise in trying to evaluate the economic impact of air pollution damage to a plant. The interrelations of time and concen- tration (dose) as they affect injury to plants are essential to air quality criteria. There are, however, only scant data relating concen- trations and length of photochemical oxi- dant exposure to chronic injury and effects on reduction of plant growth, yield, or quality. There is also a dearth of infor- mation relating concentrations to acute injury. A larger body of information exists on the acute effects of ozone, but even in this instance, the information is far from complete. Sufficient data do exist, however, to tabularly present ozone concentrations which will produce 5 percent injury to sensi- tive, intermediate, and resistant plants after a given short-term exposure, as shown in Table 10-1. Information available lists 20 species and/or varieties as sensitive, 55 as intermediate in sensitivity, and 64 as rela- tively resistant. Bacteriostatic and bacteriocidal properties of photochemical oxidants in general have been demonstrated. The growth suppression of microorganisms by ozone is a well-known phenomenon, although the ozone concen- trations for this activity are undesirable from a human standpoint. The bacteriocidal activity of ozone varies with its concen- tration, the relative humidity, and the species of bacteria. G. EFFECT OF OZONE ON MATERIALS The detailed, quantitative extent of damage to materials caused by atmospheric levels of ozone is unknown, but generally any organic material is adversely affected by concentrated ozone. Many polymers are extremely sensitive to even very small concentrations of ozone, this sensitivity increasing with the number of double bonds in the structure of the polymer. Economically, rubber is probably the most important material sensitive to ozone attack, particularly styrene-butadiene, natural, poly- butadiene, and synthetic polyisoprene. Anti- ozonant additives have been developed and are capable of protecting elastomers from ozone degradation; synthetic rubbers with inherent resistance to ozone are also available. These additives are expensive, however, and add to the cost of the end product; in addition, increasing amounts of antiozonants are required as the amount of ozone which is to be encountered increases, and sometimes only temporary protection is provided. Ozone attacks the cellulose in fabrics through both a free radical chain mechanism and an electrophilic attack on double bonds; light and humidity appear necessary for ap- preciable alterations to occur. The relative susceptibility of different fibers to ozone attack appears to be, in increasing order, cotton, acetate, nylon, and polyester. Table 10-1. PROJECTED OZONE CONCENTRATIONS WHICH WILL PRODUCE, FOR SHORT-TERM EXPOSURES, 5 PERCENT INJURY TO ECONOMICALLY IMPORTANT VEGETATION GROWN UNDER SENSITIVE CONDITIONS Time, hi 0.2 0.5 1.0 2.0 4.0 8.0 Ozone concentrations producing injury in three types of plants, ppm Sensitive 0.35-0.75 0.15-0.30 0.10-0.25 0.07-0.20 0.05-0.15 0.03-0.10 Intermediate 0.70-1.00 0.25-0.60 0.20-0.40 0.15-0.30 0.10-0.25 0.08-0.20 Resistant 0.90 and up 0.50 and up 0.35 and up 0.25 and up 0.20 and up 0.15 and up 10-4 ------- Certain dyes are susceptible to fading during exposure to ozone. The rate and extent of fad- ing is also dependent upon other environmental factors such as relative humidity and the presence of air pollutants other than ozone, as well as the length and concentration of ozone exposure and the type of material exposed. H. TOXICOLOGICAL STUDIES OF PHOTOCHEMICAL OXIDANTS 1. Effects of Ozone in Animals The major physiological effects of ozone are on the respiratory system. Inhalation of ozone at concentrations greater than about 5,900 pg/m3 (3 ppm) for several hours pro- duces hemorrhage and edema in the lungs. This reaction can be fatal to animals. Rats and mice appear to be more sensitive than rabbits, cats, and guinea pigs. The toxicity is greater for young animals and for exercising animals. It is abated by intermittency of exposure, by prophylactic administration of chemical re- ducing agents, or by introducing agents into the diet which reduce the activity of the thyroid gland. At exposures less than those which produce edema in the lungs, changes in the mechanical properties of the lung occur. These are accompanied by increased breathing rates and increased oxygen consumption. Re- peated non-fatal exposures to concentrations greater than 15,700 jug/m3 (8 ppm) for 30 minutes have produced fibrosis in the respira- tory tract of rabbits, with the damage increas- ing in severity over the length of the respira- tory tract from the trachea to the bronchioles. Short-term exposures to ozone also pro- duce chemical changes in the lung tissue ele- ments of animals. A study conducted on a small number of rabbits showed that inhala- tion of 1,960 to 9,800 Mg/m3 (1 to 5 ppm) ozone for 1 hour can produce denaturation of the structural lung proteins. Ozone also ap- pears to oxidize the sulfhydryl groups of amino acids in the lung. Short-term exposures to ozone also pro- duce changes in organs other than the lung. Concentrations of 5,900 jug/m3 (3 ppm) for 20 hours can stimulate some adaptive liver enzymes. Inhalation of 390 to 490 (0.2 to 0.25 ppm) ozone for 30 to 60 minutes makes the red blood cells of mice, rabbits, rats, and man more sensitive to the shape-al- tering effects of' irradiation. Exposure of blood to ozone in vitro produces interference with the release of oxygen from red blood cells; this suggests that ozone exposure could impair the delivery of oxygen to the tissues. Ozone exposures at concentrations from 1,310 to 7,800 jug/m3 (0.67 to 4.0 ppm) have been shown to reduce the in vitro phagocytic abilities of the pulmonary alveolar macrophag- es. A 3-hour exposure to 9,800 jug/m3 (5 ppm) ozone has been shown to reduce the activity of bactericidal enzyme, presumably due to in vivo oxidation of the enzyme. Ozone inhalation increases the vulnerability of animals to other agents. A single exposure to ozone at a concentration of 160 jug/m3 (0.08 ppm) for 3 hours has increased the mortality among mice from inhalation of pathogenic bacteria. This occurred when the bacteria were administered both before and after exposure to ozone. Ozone also increases the toxicity of histamine in guinea pigs. Long-term effects of ozone exposure in- clude, in some species, the development of tolerance to biological effects of ozone, production of fibrotic changes in the lungs, and a possible increase in the rate of aging. While tolerance has been shown in rodents, it has not been shown in chickens, and it is not certain whether or not it occurs in man. In species where tolerance to ozone exposure has been demonstrated, information is not avail- able concerning the duration and mechanism of tolerance following repeated exposure. The aging effect may be similar to the changes produced by exposure to free radicals or by irradiation. 2. Effects of Ozone in Humans Some studies of human exposures to ozone have focused on the determination of the threshold level at*which odor can be detected, and on the occurrence of changes in pulmo- nary function. Nine out of 10 subjects ex- posed to 40 pig/m3 (0.02 ppm) ozone were able to detect the odor immediately, and it 10-5 ------- persisted for an average of 5 minutes. Thir- teen of 14 subjects exposed to 100 pg/m3 (0.05 ppm) ozone indicated the odor is considerably stronger at this concentration, and the odor persisted for an average of 13 minutes. Occupational exposure of humans to ozone concentrations of up to 490 jug/m3 (0.25 ppm) has not produced detectable changes in pulmonary function. Respiratory symptoms and a decrease in vital capacity in three out of seven smokers who had been occupationally exposed to ozone have occurred at concentra- tions greater than 590 jug/m3 (0.3 ppm). Experimental exposures of humans have been carried out at concentrations ranging from 200 to 7,800 /ug/m3 (0.1 to about 4 ppm) for periods of up to 2 hours. Exposure to 390 ng/m3 (0.2 ppm) for 3 hours daily, 6 days a week, for 12 weeks has not produced any change in ventilatory function tests. Similar exposure to 980 jug/m3 (0.5 ppm) produced a decrease in the forced expiratory volume during the last 4 weeks of exposure, with recovery taking place in a subsequent 6-week period. In each of 11 subjects, expo- sure to 1,180 to 1,570 jug/m3 (0.6 to 0.8 ppm) for 2 hours resulted in an impairment of the diffusing capacity of the lung. Small decreases in vital capacity and forced expira- tory volume were observed in some of these subjects. Resistance to flow of air in the respiratory tract increased slightly in some sub- jects after exposure to 200 to 1,180 /ug/m3 (0.1 to 0.6 ppm) for 1 hour, and increased con- sistently in each of four subjects after exposure to 1,960 Mg/m3 (1 ppm) for 1 hour. Data obtained from animal experimenta- tion cannot be used directly to define the ozone concentrations above which human health will be affected. Animal mortality studies, however, can be useful in determining the factors involved in toxicity. While the concentrations of ozone used in the deter- mination of short-term non-fatal effects in animals are rarely found in ambient air, the changes in pulmonary function observed dur- ing and after exposure to these concentrations call attention to the possibility that similar effects may be observed in humans. When interpreting the research conducted thus far using human subjects, it must be noted that occupational exposures differ from experimental exposures, because it is difficult in an occupational environment to define the exact nature and dose of the pullutants present. 3. Effects of Peroxyacetyl Nitrate Experimental studies with peroxyacetyl ni- trate (PAN) in animals indicate that mortality may be delayed for 7 to 14 days after exposure; however, the exposure levels requir- ed to produce this mortality never occur in ambient atmospheres. A single experimental study of healthy human subjects exposed to 1,485 jug/m3 (0.3 ppm) peroxyacetyl nitrate indicated only that there may be a small increase in oxygen uptake with exercise. Sensitive pulmonary function tests were not obtained. The data from animal and human studies are sparse and inadequate for determining the toxicological potential of peroxyacetyl ni- trate. It would appear, however, that at the concentrations of this compound known to occur in ambient atmospheres, PAN does not present any recognized health hazard. 4. Effects of Mixtures Containing Photo- chemical Oxidants on Animals Studies have been conducted on animals exposed to both synthetic and natural photo- chemical smog. Synthetic smog has been produced by the irradiation of diluted motor vehicle exhaust or by irradiation of air mix- tures containing nitrogen oxides and certain hydrocarbons. Exposures to irradiated motor vehicle exhaust are complicated by the simul- taneous presence of carbon monoxide and other non-oxidant substances which include high concentrations of formaldehyde. Guinea pigs show increased respiratory volume during a four-hour exposure to irradiated exhaust containing 1,570 /ig/m3 (0.8 ppm) total oxidant. 10-6 ------- Exposure of mice to both natural and synthetic smog for 3 hours, at concentrations greater than 780 Mg/m3 (0.4 ppm) oxidants have produced changes in the fine structure of the lung. The nature and extent of the damage was the same after exposure to either type of smog with the same oxidant levels. The severity of the damage increased with age and became irreversible at age 21 months. Chronic exposure of guinea pigs to ambient air with an average oxidant concentration of from 40 to 140 Mg/m3 (0.02 to 0.07 ppm) leads to a significant increase in flow resist- ance when the peak oxidant concentrations exceed 980 Mg/m3 (0-5 ppm). When male mice, prior to mating, were given long-term exposures to irradiated auto exhaust containing from 200 to 1,960 /-tg/m3 (0.1 to 1.0 ppm) oxidant, a decrease in fertility and an increase in neonatal mortality of their offspring resulted; the irradiated mixture also contained varying concentrations of carbon monoxide, nitrogen oxides, and hydrocarbons. Similar exposures also cause a reduction in spontaneous running activity, which results in an adaptation response. Thus a number of experimental studies have demonstrated that changes in lung tissue or lung function occur when animals are exposed for several hours to photo-oxidized mixtures containing 980 Mg/m3 (0.5 ppm) or more of oxidants. 5. Effects of Mixtures Containing Photo- chemical Oxidants on Humans Laboratory studies of human exposure to photochemical smog have involved primarily the measurement of eye irritation. Based on the existing data, it appears that: (1) the effective eye irritants are the products of photochemical reactions; (2) although oxi- dant concentrations may correlate with the severity of eye irritation, a direct cause-effect relationship has not been demonstrated since ozone, the principal contributor to ambient oxidant levels is not an eye irritant; (3) the precursors of the eye irritants are organic compounds in combination with oxides of nitrogen, the most potent being aromatic hydrocarbons; (4) the chemical identities of the effective irritants in synthetic systems are known as being formaldehyde, peroxybenzoyl nitrate (PBzN), peroxyacetyl nitrate (PAN), and acrolein, although the latter two contri- bute to only a minor extent; and (5) the substances causing eye irritation in the atmo- sphere have not been competely defined. I. EPIDEMIOLOGICAL STUDIES OF PHO- TOCHEMICAL OXIDANTS Several studies have examined daily mortal- ity rates in localities where photochemical air pollution occurs, to determine if a relation- ship exists with increased levels of oxidant. Such an association has not been shown. These studies, however, pose a number of unresolved questions. One of these is, what is the effect of temperature, either alone or in combination with oxidants? In some of the most severe episodes, there has been an associated increase in environmental tempera- ture, sufficient to cause excess mortality by itself. Several studies of mortality among resi- dents in nursing homes in Los Angeles showed such excess mortality. In recent heat wave and air pollution episodes, however, large proportions of the elderly and ill persons in nursing homes have been protected by air conditioning. Evidence of increased morbidity has been sought through study of general hospital admissions, but no unequivocal association between photochemical air pollution and in- creased morbidity has been shown. Additional studies are indicated for improved definition. Peak oxidant values of 250 //g/m3 (0.13 ppm), which might be expected in relation to maximum hourly average levels of 100 to 120 /jg/m3 (0.05 to 0.06 ppm), have been associa- ted with aggravation of asthma. No associa- tion between ambient oxidant concentrations and changes in respiratory symptoms or func- tion was shown, however, in two separate studies of subjects with preexisting chronic respiratory disease. Non-smoking subjects with chronic respiratory disease did, however, demonstrate less airway resistance when they were studied in a room where the ambient air 10-7 ------- of Los Angeles was filtered before entry. No acute or chronic effects of oxidant pollution on ventilatory performance of elementary schoolchildren were demonstrated in a study conducted in two communities within the Los Angeles basin. Impairment of performance by high school athletes has been observed when photochemi- cal oxidants ranged from 60 to 590 /ug/m3 (0.03 to 0.3 ppm) for 1 hour immediately prior to the start of activities. Significantly, more automobile accidents have also occurred on days of high oxidant concentrations, but no threshold level for this effect could be determined from the analysis. Among the general community, eye irrita- tion is a major effect of photochemical air pollution. In Southern California, it has af- fected more than three-fourths of the popula- tion. Eye irritation under conditions prevalent in Los Angeles is likely to occur in a large fraction of the population when oxidant concentrations in ambient air increases to about 200 jug/m3 (0.10 ppm). This oxidant value might be expected to be associated with a maximum hourly average oxidant concen- tration of 50 to 100 Mg/m3 (0.025 to 0.50 ppm), depending on localized conditions. According to survey data gathered in 1956, asthma, cough, and nose and throat com- plaints were more frequent in Los Angeles, Orange, and San Diego counties than in the San Francisco Bay area or in the rest of the State. Casual reports of the presence of the symptoms of eye irritation have been record- ed in many cities in the United States. Epidemiologic studies have been inadequate, however, to relate these symptoms clearly to measured exposures to photochemical oxi- dants. In fact, one of the major photochemi- cal oxidants, ozone, is not an eye irritant. That eye irritation is experienced whenever the oxidant level exceeds a certain value is an indication that oxidant concentrations corre- late well with other aspects of the photo- chemical complex; oxidant levels are probably a measure of the photochemical activity which produces the eye irritants. On the other hand, it must be recognized that reactions of ozone with hydrocarbons do lead to hydro- carbon fragments which are eye irritants. Nor can the possibility be discounted that ozone in the photochemical complex may exert a synergistic effect on eye irritation. Because the oxidant reading measured only the net oxidizing property of the atmosphere, how- ever, the same amount of eye irritation experienced in two different geographical locations from identical irritants could be associated with different levels of oxidant, if other pollutants differed in their concentra- tion. J. AREAS FOR FUTURE RESEARCH 1. Environmental Aspects of Photochemical Oxidants 1. Research should be conducted to further identify the substance(s) which cause eye irritation. 2. The nature of the photochemical aero- sol, its behavior at different pressures of water vapor, and the nature of the surface layer of the particulates remains to be determined. 3. The role of sulfur dioxide in the forma- tion of photochemical aerosols and in the impairment of visibility should be investigated. 4. Mechanisms of photochemical oxidant formation should be explained. 2. Toxicity of Ozone, Photochemical Oxidants, and Peroxyacyl Nitrates l.The effect of ozone and PAN in combination with other pollutants found in ambient air should be investigated. Considerable information is available on the separate effects of ozone, nitrogen dioxide, and sulfur dioxide, but data on the combined effects of defined concen- trations of these gases are sparse. The effect of particulates (dust, saline drop- lets, oil, soots, etc.) should be deter- mined alone and in combination with the gases. Additional variables such as 10-8 ------- humidity and temperature should be controlled and recorded. These experi- ments should be carried out with materi- als, vegetation, animals, and, under ap- propriate conditions, in man. 2. Experiments with human exposures to gas mixtures should include a compari- son between the respiratory effects shown in healthy subjects and those shown in patients with chronic respira- tory disease, care being taken to respect the rights of experimental subjects. 3. Existing data demonstrate that tolerance occurs only in rodents. Indices other than mortality are required to demon- strate tolerance in animals. If such in- dices can be developed, then a study is needed to see if a similar phenomenon occurs in man. 4. The mechanisms of systemic effects of ozone (headache, fatigue, impaired oxy- gen transport by hemoglobin, inability to concentrate, etc.) have yet to be explained. 5. The rate and site of uptake of ozone and its fate following uptake should be deter- mined in vegetation and animals. 6. The mechanism for the production of ozone-induced pulmonary edema re- mains unexplained. 7. Additional research in needed to define the role of peroxyacyl nitrates in the production of eye irritation. 3. Epidemiology of Photochemical Oxidants 1. Of high priority is the need to study eye and respiratory irritation in metropolitan areas outside of California. Studies should be supplemented by pulmonary function tests. 2. Although the effects of episodes of high pollution levels have been studied with respect to mortality, morbidity, impair- ment of performance, etc., additional studies are needed at different sites and for different effects. These should in- clude congenital malformations, still- births, hospitals admissions for miscar- riage, and alterations in the sex ratio of newborns. 3. The examination of children has received insufficient attention in epidemiologic studies of the health effects of air pollution. This should be undertaken with respect to the effects of photo- chemical oxidants using simple pulmon- ary function tests. Emphasis should be placed on further studies of the inci- dence of asthma attacks during episodes of high pollution. K. CONCLUSIONS Derived from a careful evaluation of the studies cited in this document, the conclu- sions given below represent the best judgment of the scientific staff of the National Air Pollution Control Administration of the ef- fects that may occur when various levels of photochemical oxidants are reached in the ambient air. The more detailed information from which the conclusions were derived, and the qualifications that entered- into the con- sideration of these data, can be found in the appropriate chapter of this document. 1. Human Exposure a. Ozone (1) Long-term exposure of human subjects. (a) Exposure to a concentration of up to 390 /ig/m3 (0.2 ppm) for 3 hours a day, 6 days a week, for 12 weeks, has not produced any apparent effects (Chapter 8, section B.2.) (b) Exposure to a concentration of 980 /Ltg/m3 (0.5 ppm) for 3 hours a day, 6 days a week, has caused a decrease in the 1-second forced expiratory volume (FEVli0) after 8 weeks (Chapter 8, section B.2) (2) Short-term exposure of human subjects. (a) Exposure to a concentration of 40 Mg/m3 (0.02 ppm) was detected immediately by 9 of 10 subjects. 10-9 ------- After an average of 5 minutes expo- sure, subjects could no longer detect ozone (Chapter 8, section E.2). (b) Exposure to a concentration of 590 jug/m3 (0.3 ppm) for 8 hours appears to be the threshold for nasal and throat irritation (Chapter 8, section E.2.) (c) Exposure to concentrations of from 1,180 to 1,960 jug/m3 (0.6 to 1.0 ppm) for 1 to 2 hours may impair pulmonary function by causing in- creased airway resistance, decreased carbon monoxide diffusing capacity, decreased total capacity, and de- creased forced expiratory volume (Chapter 8, section B.2'.) (d) Exposure to concentrations of from 1,960 to 5,900 Mg/m3 (1.0 to 3.0 ppm) for 10 to 30 minutes is in- tolerable to some people (Chapter 5, section B.2.) (e) Exposure to a concentration of 17,600 Mg/m3 (9.0 ppm) produces severe illness (Chapter 5, section B.2.) b. Oxidants (1) Long-term exposure of human subjects. Exposure to ambient air containing an oxidant concentration of about 250 /ig/m3 (0.13 ppm) (maximum daily value) has caused an increase in the number of asthmatic attacks in about 5 percent of a group of asthmatic patients. Such a peak value would be expected to be associated with a maximum hourly average concentration of 100 to 120jug/m3 (0.05 to 0.06 ppm) (Chapter 9, section B.3.) (2) Short-term exposure of human subjects. (a) Exposure to an atmosphere with peak oxidant concentrations of 200 /ig/m3 (0.1 ppm) and above has been asso- ciated with eye irritation. Such a peak concentration would be expected to be associated with a maximum hourly average concentration of 50 to 100 /zg/m3 (0.025 to 0.05 ppm) (Chapter 9, section B.3.) (b) Exposure to an atmosphere with aver- age hourly oxidant concentrations ranging from 60 to 590 Mg/m3 (0.03 to 0.30 ppm) has been associated with impairment of performance of stu- dent athletes (Chapter 9, section B.4.) 2. Other Exposures a. Photochemical Oxidants (1) Effects on vegetation and laboratory animals. (a) Exposure to concentrations of about 60 Mg/m3 (0.03 ppm) ozone for 8 hours or to 0.01 ppm peroxyacetyl nitrate for 5 hours has been associa- ted with the occurence of leaf lesions in the most sensitive species, under laboratory conditions (Chapter 6, sec- tion E.) (b) Exposure to ambient air containing oxidant concentrations of about 100 Mg/m3 (0.05 ppm) for 4 hours has been associated with leaf injury to the most sensitive species (Chapter 6, section E.) (c) Experimental exposures of laboratory animals to ozone concentrations of from 160 to 2,550 MS/m3 (0.08 to 1.30 ppm) for 3 hours has resulted in increased susceptibility to bacterial infection (Chapter 8, section B.I.) b. Ozone Effects on Susceptible Materials (1) Polymers. (a) Many polymers, especially rubber, are extremely sensitive to very small con- centrations. To provide protection, antiozonant additives are used, but are expensive and add to the cost of the end product (Chapter 7). (2) Cellulose and dyes. (a) The cellulose in fabrics is attacked by ozone, with subsequent weakening of the fabric. Similarly, certain dyes are susceptible to fading during exposure to ozone (Chapter 7). Tables 10-2 10-10 ------- Table 10-2. EFFECTS OF OZONE Effect Vegetation damage2 Cracking of stretched rubber Odoi detection Increased susceptibility of laboratory animals to bacterial infection Respiratory irritation (nose and throat), chest constriction Changes in pulmonary function: Diminished FEVj Q after 8 weeks Small decrements in VC, FRC, and DL^jQ in, respectively ,3, 2, and 1 out of 7 subjects Impaired diffusion capacity (DL^Q) Increased airway resistance Reduced VC, severe cough, inability to concentrate Acute pulmonary edema Exposure ppm 0.03 0.02 0.02 0.08 to 1.30 0.30 0.50 0.20 to 0.30 0.60 to 0.80 0.10 to 1.00 2.00 9.00 ttgjm3 60 40 40 160 to 2,550 590 980 390 to 590 1,180 to 1,570 200 to 1,960 3,900 17,600 Duration 8 hours 1 hour <5 minutes 3 hours Continuous during working hours 3 hours/day, 6 days/week, for 12 weeks Continuous during working hours 2 hours 1 hour 2 hours Unknown Comment Sensitive species; laboratory conditions Vulcanized natural rubber Odor detected in 9 of 10 subjects Demonstrated in mice at 160 fig/m and in mice at 2550 Mg/m3 Occupational exposure of welders, other pollutants probably also present Experimental exposure of 6 subjects. Change returns to normal 6 weeks after exposure. No changes observed at 390^g/m3 (0.2 ppm) Occupational exposure. All 7 subjects smoked. Normal values for VC, FRC, and DLCO based on predicted value. Experimental exposure of 11 subjects Significant increase in 2 of 4 subjects at 200 Mg/m3 (0.1 ppm) and 4 of 4 subjects at 1960Mg/m3(1.0ppm) High temperatures. One subject. Refers to peak concentration of occupa- tional exposure. Most of exposure was to lower level Reference Heck and Dunning Bradley and Haagen-Smit Henschler et al. Coffin et al. Miller et al. Kleinfeld et al. Bennett Young et al. Young et al. Goldsmith et al. Griswold et al. Kleinfeld et al. Similar vegetation damage also occurs upon exposure to 0.01 ppm peroxyacetyl nitrate for 5 hours. ------- o to Table 10-3. EFFECTS ASSOCIATED WITH OXIDANT CONCENTRATIONS IN PHOTOCHEMICAL SMOG Effect Vegetation damage Eye irritation Aggravation of respiratory diseases- asthma Impaired performance of stu- dent athletes Exposure, ppm 0.05 Mg/m3 100 Exceeding 0.1 0.13a 0.03 to 0.30 200 250 60 to 590 Duration 4 hours Peak values Maximum daily value 1 hour Comment Leaf injury to sensitive species Result of panel response. Such a peak value would be expected to be associated with a maximum hourly average concentration of 50 to 100 Mg/m3 (0.025 to 0.05 ppm) Patients exposed to ambient air. Value refers to oxidant level at which number of attacks increased Such a peak value would be expected to be associated with a maximum hourly average concentration of 100 to 120 Mg/m (0.05 to 0.06 ppm). Exposure for 1 hour immediately prior to race Reference MacDowall et al Renzetti and Gobran Schoettlin and Landau Wayne et al. ^Calculated from a measured value of 0.25 ppm (phenolphthalein method) which is equivalent to 0.13 ppm by the KI method. ------- and 10-3 present these conclusions in tabular form. L. RESUME' Under the conditions prevailing in the areas where studies were conducted, adverse health effects, as shown by impairment of perfpr- mance of student athletes, occurred over a range of hourly average oxidant concentra- tions from 60 to 590 jug/m3 (0.03 to 0.3 ppm). An increased frequency of asthma attacks in a small proportion of subjects with this disease was shown on days when oxidant concentrations exceeded peak values of 250 jug/m3 (0.13 ppm), a level that would be associated with an hourly average concentra- tion ranging from 100 to 120jug/m3 (0.05 to 0.06 ppm). Adverse health effects, as mani- fested by eye irritation, were reported by subjects in several studies when photochemi- cal oxidant concentrations reached instan- taneous levels of about 200 pg/m3 (0.10 ppm), a level that would be associated with an hourly average concentration ranging from 60 to 100 jug/m3 (0.03 to 0.05 ppm). Adverse effects on sensitive vegetation were observed from exposure to photochemical oxidant concentrations of about 100 /ug/m3 (0.05 ppm) for 4 hours. Adverse effects on materials from exposure to photochemical oxidants have not been precisely quantified, but have been observed at the levels presently occurring in many urban atmospheres. It is reasonable and prudent to conclude that, when promulgating ambient air quality standards, consideration should be given to requirements for margins of safety that would take into account possible effects on health, vegetation, and materials that might occur below the lowest of the above levels. 10-13 ------- AP-63 ERRATA FOR AIR QUALITY CRITERIA FOR PHOTOCHEMICAL OXIDANTS (Summary and Conclusions) Page 10-7, col. 2, section I, par. 2, lines 7-11: change to read: "Peak oxidant values ot 4yu ug/m^ (u.tb ppmj, wnich might be expected in relation to a maximum hourly average level as low as 300 ug/m3 (0.15 ppm) have been associated with aggravation of asthma." Page 10-8, section I, col. 1, par. 2, lines 3 and 4: change "ranged from 60 to 590 ug/m3 (0.03 ppm to 0.3 ppm)" to read "exceeded 130 ug/m3 (0.07 ppm)" Page 10-8f section If col. 1. par. 2. lines 9-13: delete sentence "This oxidant value...localized conditions." Page 10-10f col. lf section l.b.fl). lines 2 and 3: change "250 ug/m3 (0.13 ppm)" to read "490 ug/rn^ (0.25 ppm)" Page 10-10. col. 1. section l.b.(l), lines 9 and 10: change "of 100 to 120 ug/m3 (0.05 to 0.06 ppm)" to read "as low as 300 ug/m3 (0.15 ppm)" Page 10-10, col. 1 and 2, section l.b.(2) (a), lines 4-7: delete sentence beginning "Sucli a peak..." " Page 10-10. col. 2, section l.b.(2)(a), lines 1 and 2: add "(Chapter 9, section B.5.)" to end of previous sentence ( in column 1). Page 10-10. col. 2, section l.b.(2)(b), lines 3 and 4: change "ranging from 60 to 590 ug/m3 (0.03 to 0.30 ppm)" to read "in excess of 130 ug/m3 (0.07 ppm)" Page 10-12, Table 10-3, column 5, third comment: delete comment "Such a peak value...(0.025 to 0.05 ppm)." Page 10-12, Table 10-3, column 2, entry 5: change "0.13a" to read "0.25" Page 10-12, Table 10-3, column 3, entry 3: change "250" to "490" (OVER) ------- Page 10-12, Table 10-5, column 5, fifth comment, lines 3 and 4: change "of 100 to 120 ug/m3 (0.05 to 0.06 ppm)" to read "as low as 300 ug/m3 (0.15 ppm)" Page 10-12 Table 10-3, columns 2 and 3, fourth entry: Add the word "Exceeding" (as above Tor eye irritation) Page 10-12, Table 10-3, column 2, fourth entry: change "0.03 to 0.30" to "0.07" Page 10-12, Table 10-5. column 3. fourth entry: change "60 to 590" to "130" Page 10-12, Table 10-3, footnote: delete footnote. Page 10-13, col. 1, section L, par. 1. lines 4-6: change "over a range of hourly average oxidant concentrations from 60 to 590 ug/m3 (0.03 to 0.3 ppm)" to read "when the hourly average oxidant concentrations exceeded 130 ug/m3 (0.07 ppm)" Page 10-13, col. 1, section L, par. 1, lines 10 and 11: change "250 ug/m3 (0.13 ppm)"to "490 ug/m-5 (0,25 ppm)" Page 10-15, col. I, sectign L, par. 1, lines 13 and 14: change "ranging from 100 to 120 ug/m5 (0.05 to 0.06 ppm) to read "as low as 300 ug/m3 (0.15 ppm)." Page 10-15, section L, col. 2, par. 1, lines 3-5: delete "a level that... (0.03 to 0.05 ppm)". JCR/ps/9-17-70 ------- |